Viral Historians

Researchers at UB trace the ancestry of some of Earth’s most dangerous viruses

“The viral-host interaction is such an important interaction for all life on this planet, but it’s kind of a huge missing area of biology.”

Derek Taylor

To study Ebola and Marburg viruses, researchers must don
airtight suits and lock themselves in a biocontainment lab,
separated from the outside world by decontamination showers. The
viruses cause hemorrhagic fevers in humans; victims bleed from the
eyes, ears, mouth and other orifices.

Ebola and Marburg belong to a family of viruses called
filoviruses. Experts once believed these lethal agents were less
than 10,000 years old, but recent UB research pushed the age
back—way back—to at least 10 million years.

UB biologists Jeremy Bruenn and Derek Taylor, the study’s
leaders, investigate “fossil genes”: chunks of genetic
material, often sizable, that animals and other organisms
“steal” from viruses. The partners found remnants of
filovirus genes in a lot of small mammals, including a Buffalo Zoo
wallaby and a bat caught at UB. In mice and rats, the genes
appeared in the same spot in the genome, meaning the material was
likely acquired in ancient times, before the animals evolved as
distinct species.

“A viral gene being inserted independently at the exact
same position in different species is highly unlikely, so it must
have happened in a common ancestor,” Taylor explains. The
finding is one of many surprising results emerging from Taylor and
Bruenn’s work.

Until recently, many researchers—including Taylor and
Bruenn—didn’t think it was possible for filoviruses to
leave their imprint on host DNA at all. That’s because
filoviruses are non-retroviral RNA viruses, which lack the genetic
machinery to produce reverse transcriptase, an enzyme needed for
copying viral material into host genomes.

Bruenn changed his thinking in 2005, when he saw fossil genes
from a non-retroviral RNA virus in two species of yeasts.
“Not only were they there, but they appeared to be
functional,” Bruenn recalls. “I was really intrigued:
How did they get there, and why were they there?”

Now, he and Taylor are zeroing in on answers. Their research
suggests that viral material gets into host DNA because of reverse
transcriptase already present in the cells of the host. As for why
organisms retain viral genes, Bruenn posits that doing so may
confer antiviral resistance.

Moving forward, the researchers will use fossil genes to better
pinpoint the age and origin of dangerous viruses. “The
viral-host interaction is such an important interaction for all
life on this planet, but it’s kind of a huge missing area of
biology,” says Taylor. “We don’t have a lot of
information about what happened in deep time.”

Next Steps

Since publishing on Ebola and Marburg in 2010, Bruenn and Taylor
have worked with UB colleagues to identify viral remnants in a
plethora of organisms, including plants and fungi. The team found
that the fruit fly Drosophila has fossil genes, a notable discovery
because the insects breed quickly and—like fast-replicating
yeasts— could be used to study the purpose of amassing viral
material.